(P37-11-26) Associations of Early Childhood Added Sugar Intake With Abdominal and Hepatic Fat Trajectories Through Adolescence

Monday, July 27, 2026

9:30 AM - 10:30 AM ET

Location: Poster Board C-45

Presenting Author(s)

Catherine C. Cohen, PhD, RDN (she/her/hers)

Assistant Professor
University of Colorado Denver
Denver, Colorado, United States

Co-Author(s)

EE

Erin K. Englund

University of Colorado Anschutz Medical Campus, United States
JG

Jason Giles

University of Colorado Anschutz Medical Campus, United States
DG

Deborah H. Glueck, PhD

University of Colorado Anschutz Medical Campus
Aurora, Colorado, United States
LL

Leslie Lange

University of Colorado Anschutz Medical Campus, United States
MK

Megan M. Kelsey

University of Colorado Anschutz Medical Campus, United States
DD

Dana Dabelea, MD, PhD

Conrad M. Riley Endowed Professor of Epidemiology, Professor of Pediatrics, and Director of the Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center)
University of Colorado Anschutz Medical Campus
Aurora, Colorado, United States

Disclosure(s):

Catherine C. Cohen, PhD, RDN: No relevant financial relationship(s) with ineligible companies to disclose.

Objectives: Hepatic fat (HF) is a strong risk factor for insulin resistance, driven by environmental and genetic factors, including the PNPLA3 rs738409 allele. Higher added sugar intake, especially from sugar‑sweetened beverages (SSBs), in adolescence has been linked to HF deposition, but its influence earlier in childhood, and whether this differs by genotype, remains unclear. We examined the independent and joint associations of early‑childhood added sugar intake and PNPLA3 genotype with HF trajectories from childhood to adolescence.

Methods: Participants were 403 children in the Colorado Healthy Start Study, a longitudinal cohort, who completed magnetic resonance imaging (MRI) to assess HF in early childhood (~5 y), mid childhood (~9 y), and/or early adolescence (~12 y). Added sugar (%kcal/d) and SSB intake (servings/d) were assessed in early childhood using 24-hour recalls. PNPLA3 genotyping was also performed in a subset (n=299, 74%). Linear mixed models examined associations of diet and genetic risk factors with log-transformed HF trajectories from childhood to adolescence. Due to a high percentage (62%) of participants reporting zero SSB intake in early childhood, we analyzed SSB intake as a categorical variable (any vs. none).

Results: Mean HF increased from early childhood (Geometric Mean: 1.65%) to adolescence (2.30%). In linear mixed models adjusted for sex, there was no significant association between added sugar intake in early childhood and HF trajectories. However, any SSB intake in early childhood, versus none, was associated with higher HF in middle childhood (back transformed β [95% CI]: 1.11 [1.00, 1.24]) and adolescence (β< [95% CI]: 1.22 [1.02, 1.46]) but not concurrent HF at baseline (p=0.78). Participants who were homozygous or heterozygous for the PNPLA3 risk allele (GG=6%, GC=38%) had significantly higher HF across all visits (p < 0.05). We did not find significant differences in diet-HF associations by PNPLA3 genotype (interaction p >0.05).

Conclusions: In this general risk cohort, early childhood SSB intake predicted greater HF accumulation later in childhood/adolescence, suggesting this may be a key target for future prevention strategies. PNPLA3 risk‑allele carriers had higher HF overall, but we did not find statistically significant diet-by-gene interactions.

Funding Sources: NIH/NIDDK